The anti-diuretic hormone vasopressin (AVP) regulates water excretion
from the kidney by increasing the water permeability of the collecting
duct. AVP binds to V-2-receptors and induces the translocation of aqu
aporin-2 water channels (AQP-2) into the apical plasma membrane of pri
ncipal cells. By this mechanism AVP controls water reabsorption in the
kidney. The effects of AVP on the endolymphatic sac (ES) of the inner
ear, which is thought to mediate reabsorption of endolymph, were inve
stigated. Both the V-2-receptor and the AQP-2 water channel were found
to be expressed in the ES epithelium. In the ES AVP binds to receptor
s most probably of the V-2-subtype. Application of AVP to organotypica
lly cultured ES inhibits membrane turnover in ribosomal-rich cells of
the ES epithelia, which is thought to mediate translocation of AQD-2 i
nto the surface membrane. This suggests that AVP has contrasting effec
ts in the inner ear and kidney, which may be physiologically useful fo
r maintaining endolymphatic pressure during severe hypovolemia. Animal
experiments show that AVP causes endolymphatic hydrops after systemic
application to guineapigs, which suggests a causal role for the incre
ased AVP levels found in humans suffering from Meniere's disease.